Effect of DEC1 on the proliferation, adhesion, invasion and epithelial‑mesenchymal transition of osteosarcoma cells

Abstract

Differentiated embryonic chondrocyte-expressed gene 1 (DEC1) is associated with various types of human cancer; however, there is limited data regarding the functions of DEC1 in osteosarcoma. The present study aimed to examine the expression of DEC1 in human osteosarcoma tissues and cell lines. Furthermore, the effects of DEC1 on the proliferation, adhesion, invasion and epithelial-mesenchymal transition (EMT) of osteosarcoma cells were investigated. Using reverse transcription-quantitative PCR and western blot analysis, it was found that the expression levels of DEC1 were higher in human osteosarcoma tissues and osteosarcoma cell lines than in the controls. Both gain-and loss-of-function experiments suggested that DEC1 promotes the proliferation, adhesion and invasion of osteosarcoma cells in vitro, as determined by MTT, cell adhesion and cell invasion assays, respectively. Additionally, DEC1 was found to upregulate the mesenchymal markers N-cadherin and vimentin, whilst downregulating the epithelial marker E-cadherin. In conclusion, this present study showed increased expression levels of DEC1 in human osteosarcoma tissues and cell lines, and identified that DEC1 may exert its effect on osteosarcoma progression by promoting cell proliferation, adhesion and invasion. Furthermore, DEC1 was shown to have an inducible effect on EMT in osteosarcoma cell lines, thus contributing to the aggressiveness of osteosarcoma cells. This initial study indicated that DEC1 may serve as a novel molecular target for the treatment of osteosarcoma.

Expression of E-cadherin and N-cadherin in Epithelial-to-Mesenchymal Transition of Osteosarcoma: A Systematic Review

“…The expression of E-cadherin was closely inversely related to the expression of N-cadherin, which predicted the malignant potential and invasiveness of osteosarcoma cell lines [27][28][29]. Several studies in this article concluded that upstream modification of E-cadherin expression can determine a tumor cell line's invasiveness and is associated with the severity of cancer and tumor cell survival [24][25][26].…”

“…E-cadherin expression modification has been explored as a target for therapy in multiple disease processes. In the results, multiple in vitro studies displayed a decrease in tumor malignancy and invasive potential with an increase in E-cadherin expression and a decrease in N-cadherin expression via transfection with silencing or micro RNAs targeted to upstream effectors [ 2 , 12 , 16 , 20 , 24 , 25 , 33 , 34 ]. Bi et al utilized an in vivo murine model to transfect endometrial cells with homeobox proteins that resulted in downstream upregulation of E-cadherin, improving embryo adhesion and implantation [ 46 ].…”

Circular RNA_0078767 upregulates Kruppel-like factor 9 expression by targeting microRNA-889, thereby inhibiting the progression of osteosarcoma

“…As previously described [ 24 ], the transfected MG63 and Saos2 cells were trypsinized and inoculated into 96-well plates (2 × 10 3 cells/well), and then the cells were routinely cultured. Subsequently, on days 0, 1, 2, 3 and 4, each well was added with 10 μL of 5 mg/mL MTT solution (Beyotime Biotechnology, Shanghai, China), and the cells were incubated in 5% CO 2 for 4 h at 37°C.…”

DEC1 deficiency protects against bone loss induced by ovariectomy through inhibiting inflammation

“…Differentiated embryo-chondrocyte expressed gene 1 (DEC1) is a structurally unique basic helix-loophelix (bHLH) protein which is a major regulator of a variety of physiological and pathological processes, including circadian rhythms, hypoxia, cellular proliferation, apoptosis, immunity, and inflammation [18][19][20][21][22] . Initially being identified in human chondrocytes, DEC1 is closely linked to bone growth and remodeling [23] .…”